Objective. To compare the relative safety and efficacy of auranofin (AUR), methotrexate (MTX), and the combination of both in the treatment of active rheumatoid arthritis (RA).Methods. Three hundred thirty-five patients with active RA were entered into a 48-week, prospective controlled, double-blind, multicenter trial and were randomly assigned to 1 of 3 treatment groups.Results. Two hundred eleven patients completed the trial. No remissions were seen, and there were no statistically significant differences among the treatment groups in the clinical or laboratory variables measured.Patients taking AUR alone had a slower onset of response than did patients taking MTX alone or in combination. Withdrawals because of adverse drug reactions were slightly more common for those taking combination therapy, but the differences were not statistically significant. Withdrawals because of lack of response were more common for single-drug therapy, with the difference between AUR and the combination reaching statistical significance. No unexpected adverse drug effects were identified, and all reactions resolved without sequelae. Conclusion. Except for fewer withdrawals because of lack of response, combination therapy did not demonstrate any advantage in efficacy over single-drug treatment within the time frame of the study.Clinicians usually treat rheumatoid arthritis (RA) resistant to conventional conservative management with second-line or so-called disease-modifying antirheumatic drugs. Despite numerous trials establishing the efficacy of these second-line agents compared with placebo, there is little to suggest that the relentless progression of disease is changed in those patients who are most severely affected (1,2). Controlled studies of patients with RA of long duration have established moderate efficacy over study periods that are usually less than 1 year in length, with

No abstract

Heparin-induced thrombocytopenia (HIT) is a common drug induced autoimmune condition. The thrombocytopenia is caused in most cases by an antibody directed against the complex PF4/heparin. Recently, we have induced an experimental model of HIT by idiotypic manipulation. To confirm further the idiotypic involvement of HIT, we have treated successfully three patients with HIT with high-dose intravenous gamma-globulin (IVIG). Our three patients joint other two cases previously reported who were treated with IVIG and point to the efficacy of this type of therapy with minimal side effects. IVIG suppression of the anti-PF4/heparin autoantibody may support the idiotypic etiology of HIT.

Nine azotemic patients who developed a coagulopathy associated with the use of either cephalosporin or moxalactam antibiotics are reported. The acute renal failure patients had neoplastic disorders and were considered to be septic at the time that multiple antibiotics were administered. Four of 5 chronic hemo- or peritoneal dialysis patients also received multiple antibiotics. Nevertheless, the coagulopathy seemed to be most closely associated with the administration of the cephalosporin. One patient received moxalactam as part of the combination therapy for diffuse pulmonary infiltration during renal transplant rejection. Bleeding occurred into the gastrointestinal tract in four patients, into the kidney-urinary tract in three patients, into vascular surgical sites in two patients, and one each into the pulmonary-bronchial and cerebral-ventricular systems. Five operations were performed in four patients: a nephrectomy for massive subcapsular hemorrhage with a prothrombin time that exceeded 100 seconds; arteriovenous graft complicated by post-operative bleeding associated with prolongation of the prothrombin time; elective femoral-popliteal bypass complicated by a prolonged prothrombin time, bleeding into the graft site, hypotension, and a subendocardial myocardial infarction; elective cholecystectomy complicated by a two unit bleed associated with a slightly prolonged prothrombin time, followed by elective femoral-popliteal bypass complicated by a fatal intercerebral bleed associated with a more than twice normal prothrombin time. Cephalosporins are most likely associated with Vitamin K deficiency. Moxalactam is more likely to be associated with platelet dysfunction. Monitoring of the prothrombin time for cephalosporins or the bleeding time for moxalactam is the most reliable way to prevent what may be rapid emergence of clinical bleeding in patients with renal failure.